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Abstract
Background and Aim. Calcineurin inhibitors (CNIs) have shown to develop hypertension in transplant patients. The in vitro incubation effects of cyclosporine (CsA) and tacrolimus (Tac) on vascular relaxations of rat thoracic aorta (TA) and abdominal aorta (AA) need to be investigated. Methods. The optimal concentrations of CsA (1.0 mg/mL) and Tac (0.1 mg/mL) used to compare endothelium-dependent (acetylcholine (ACh)) and endothelium-independent (sodium nitroprusside (SNP)) vascular relaxation against the agonists in phenylephrine (PE-) constricted TA and AA of 13-week-old male Sprague Dawley rats (n = 6). Results. In TA, the maximal vasodilator response elicited by ACh (control: I max 98%) was significantly (P < 0.01) inhibited by CsA (I max 10%) but not by Tac (I max 97%). In AA, (control: IC50 50 nM; I max 100%) CsA (IC50 7 μM; (P < 0.01) showed strong sensitivity to inhibit ACh-dependent vascular relaxation than Tac (IC50 215 nM (P < 0.05); I max 98%). CsA and Tac failed to affect the inhibitory responses to SNP in both TA and AA. Conclusion. CsA exerts profound inhibitory effect on endothelium-dependent vasodilatation as compared to Tac in both TA and AA. Aortic rings from the thoracic region are more sensitive to CNIs, since the vasodilator response to ACh is solely mediated by NO while in the AA, ACh likely recruits other endothelial mediators besides NO to maintain vasodilatation.
Highlights
The post-transplantation vasculopathy is an important complication after organ transplantation [1]
Either its synthesis is reduced or its increased quenching by oxidative stress is thought to result in increased vascular smooth muscle (VSM) tone and elevation in blood pressure that is accompanied by endothelial damage and loss of homeostatic regulatory property of the vascular wall [2]
The same group of investigators have demonstrated that prolonged in vivo administration of CsA leads to both endotheliumdependent (vasodilator response to acetylcholine (Ach)) as well as endothelium-independent
Summary
The post-transplantation vasculopathy is an important complication after organ transplantation [1]. Diminished NO function is thought to play a major role in the progression of post-transplantation vasculopathy [3]. Transplantation immunosuppressants such as calcineurin inhibitors (CNIs) have substantial effects on vascular reactivity, especially on NO synthesis [3]. The same group of investigators have demonstrated that prolonged in vivo administration of CsA leads to both endotheliumdependent (vasodilator response to acetylcholine (Ach)) as well as endothelium-independent The optimal concentrations of CsA (1.0 mg/mL) and Tac (0.1 mg/mL) used to compare endothelium-dependent (acetylcholine (ACh)) and endothelium-independent (sodium nitroprusside (SNP)) vascular relaxation against the agonists in phenylephrine (PE-) constricted TA and AA of 13-week-old male Sprague Dawley rats (n = 6). Aortic rings from the thoracic region are more sensitive to CNIs, since the vasodilator response to ACh is solely mediated by NO while in the AA, ACh likely recruits other endothelial mediators besides NO to maintain vasodilatation
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